Transient facial nerve palsy following dental local anaesthesia.

Facial nerve palsy is a rare but known complication of dental local anaesthesia and may be underreported. We describe a case of a transient facial nerve palsy following the administration of an inferior alveolar nerve block and discuss the immediate practical management. Knowing the likely transient nature of this complication means the patient can be reassured and unnecessary referral avoided. While the blink reflex is inhibited, steps are needed in order to protect the cornea and prevent secondary infection and scarring.

[Ophthalmic complications and local anesthesia. Pathophysiology and types of eye complications after intraoral dental anesthesia, and clinical recommendations]. / Ophthalmologische Komplikationen und Lokalanästhesie. Pathophysiologie und Formen der Augenkomplikationen nach intraoraler zahnärztlicher Lokalanästhesie und klinische Empfehlungen.

The present article reviews the different types of ophthalmologic complications following administration of intraoral local anesthesia. Since the first report by Brain in 1936, case reports about that topic have been published regularly in the literature. However, clinical studies evaluating the incidence of ophthalmologic complications after intraoral local anesthesia are rarely available. Previous data point to a frequency ranging from 0.03% to 0.13%. The most frequently described ophthalmologic complications include diplopia (double vision), ptosis (drooping of upper eyelid), and mydriasis (dilatation of pupil). Disorders that rather affect periorbital structures than the eye directly include facial paralysis and periorbital blanching (angiospasm). Diverse pathophysiologic mechanisms and causes have been reported in the literature, with the inadvertent intravascular administration of the local anesthetic considered the primary reason. The agent as well as the vasopressor is transported retrogradely via arteries or veins to the orbit or to periorbital structures (such as the cavernous sinus) with subsequent anesthesia of nerves and paralysis of muscles distant from the oral cavity. In general the ophthalmologic complications begin shortly after administration of the local anesthesia, and disappear once the local anesthesia has subsided.

Delayed facial nerve paresis following acoustic neuroma resection and postoperative vasoactive treatment.

OBJECT: Delayed facial nerve paresis is a well known clinical phenomenon following acoustic neuroma surgery, typically occurring early during the postoperative course. The clinical course of the delayed facial nerve paresis and intraoperative electromyographic (EMG) signals were evaluated in a subgroup of patients who underwent vasoactive treatment for preservation of hearing and developed secondary deterioration after termination of treatment. METHODS: Between 1990 and 2001 seven patients were identified who received vasoactive treatment for preservation of hearing and developed a delayed facial nerve paresis after termination of medication. Intraoperative facial nerve EMG activity was analyzed in six patients. RESULTS: All patients developed a delayed facial nerve paresis between 2-5 days following termination of a 10 day treatment consisting of HES and nimodipine. Medication was re-initiated and the facial nerve paresis improved in all patients. In two patients intraoperative EMG signals revealed "A-trains" waveform patterns, which are highly suggestive for an immediate postoperative facial nerve paresis, whereas in four patients no pathognomonic EMG patterns could be recorded. CONCLUSIONS: The delayed onset of a facial paresis following termination of vasoactive treatment points to a disturbed microcirculation of the nerve as the main pathophysiological feature. Two groups could be identified on the basis of intraoperative EMG activity. In one group with presence of "A-trains" medication apparently masked the onset of an immediate postoperative facial nerve deficit. Four patients without "A-trains" did not develop a typical delayed facial nerve paresis during vasoactive treatment, but thereafter. The time lag between termination of treatment and onset of a delayed palsy points to a protective effect due to improved microcirculation.

Topical papaverine and facial nerve dysfunction in cerebellopontine angle surgery.

HYPOTHESIS: Topical application of 3% papaverine hydrochloride in the cerebellopontine angle (CPA) produces reversible conduction block of the facial nerve. BACKGROUND: A case of loss of spontaneous and evoked facial muscle activity, and transient postoperative facial paralysis, after topical application of papaverine in the CPA during surgery for an acoustic neuroma using intraoperative cranial nerve monitoring is reported. Other cases of transient neurologic dysfunction after use of this drug have been reported. METHODS: A rabbit model of CPA surgery via suboccipital craniectomy, with intraoperative monitoring of the facial nerve, was used in this experiment. RESULTS: No significant difference in facial muscle stimulation thresholds was identified after application of varying concentrations of papaverine to the facial nerve in the CPA. CONCLUSION: Although the intraoperative event described in the report is suggestive of an effect of papaverine on facial nerve function, this effect could not be reproduced in an established animal model of CPA surgery.

"Sunbath polyneuritis": subacute axonal neuropathy in perazine-treated patients after intense sun exposure.

This article aims at drawing attention to the peculiar association of intense exposure to sunlight and subacute development of sensory neuropathy which was seen in 7 psychiatric patients treated with the phenothiazine derivative, perazine. Three patients additionally developed bilateral VII nerve palsy. Symptoms followed a monophasic course with almost complete remission. Routine neurophysiology suggested axonal neuropathy confirmed by sural nerve biopsy in 1 patient. A toxic origin of neuropathy is supposed, possibly induced by phenothiazine photoproducts, which may cause cell damage via lipid peroxidation.

Peripheral facial nerve paralysis after local upper dental anaesthesia.

A 50-year-old female patient developed a facial nerve paralysis after a local upper dental block. This complication is known to occur after an inferior dental block but has only sporadically been reported after local anaesthetic procedures in the upper jaw for dental treatment. Some possible pathogenetic mechanisms are discussed.

Diagnosis and treatment of complications associated with local anaesthesia.

The safety record of local anaesthetic agents is high but complications do occur. These may be systemic reactions to the local anaesthetic itself or to the vasoconstrictor. The former may be allergic or toxic in nature. Psychomotor reactions, often attributed erroneously to the vasoconstrictor, are more common. Regional complications, usually due to faulty technique, may be immediate or delayed. Among the former are pain, haematoma formation, tissue blanching, facial paralysis, amaurosis, diplopia and needle breakage. The delayed regional complications include pain, prolonged anaesthesia or paraesthesia, trismus, infection, sloughing and ulceration. The management of these complications is described.